CAJ | 학술논문

目的：研究香加皮杠柳苷（CPP）对人肺癌QG56细胞的抑制作用及其作用机制。方法体外培养人肺癌QG56细胞，设对照组和终浓度为1.25、2.50、5.00、10.00、20.00μg/L的CPP（CPP 1~5）组，每组设3个平行孔，分别培养24、48、72 h。采用MTT法检测CPP对QG56细胞增殖的影响；倒置显微镜观察CPP处理前后细胞形态变化；流式细胞术检测细胞凋亡和周期分布；RT-PCR法检测CPP作用后QG56细胞中凋亡相关基因bax mRNA表达情况；免疫细胞化学法检测CPP对QG56细胞bax蛋白表达的影响。结果随CPP浓度的增加、作用时间的延长，细胞增殖抑制率明显增高。显微镜下可见CPP处理后的QG56细胞变圆，皱缩，呈悬浮状态。随CPP浓度的增加，G0/G1期细胞比例增高，而S期和G2/M期细胞比例减少, QG56细胞凋亡率明显增高。CPP 2组经CPP作用48 h后，细胞凋亡率高于对照组，CPP 3组经CPP作用24 h后，细胞凋亡率均高于对照组，CPP 4组经CPP作用12 h后，细胞凋亡率均高于对照组（均P＜0.05）。CPP 2~4组经CPP作用48 h时QG56细胞中bax mRNA和蛋白的表达明显增强。结论 CPP可通过阻滞细胞周期和诱导凋亡发挥对人肺癌QG56细胞的抑制作用。
목적：연구향가피강류감（CPP）대인폐암QG56세포적억제작용급기작용궤제。방법체외배양인폐암QG56세포，설대조조화종농도위1.25、2.50、5.00、10.00、20.00μg/L적CPP（CPP 1~5）조，매조설3개평행공，분별배양24、48、72 h。채용MTT법검측CPP대QG56세포증식적영향；도치현미경관찰CPP처리전후세포형태변화；류식세포술검측세포조망화주기분포；RT-PCR법검측CPP작용후QG56세포중조망상관기인bax mRNA표체정황；면역세포화학법검측CPP대QG56세포bax단백표체적영향。결과수CPP농도적증가、작용시간적연장，세포증식억제솔명현증고。현미경하가견CPP처리후적QG56세포변원，추축，정현부상태。수CPP농도적증가，G0/G1기세포비례증고，이S기화G2/M기세포비례감소, QG56세포조망솔명현증고。CPP 2조경CPP작용48 h후，세포조망솔고우대조조，CPP 3조경CPP작용24 h후，세포조망솔균고우대조조，CPP 4조경CPP작용12 h후，세포조망솔균고우대조조（균P＜0.05）。CPP 2~4조경CPP작용48 h시QG56세포중bax mRNA화단백적표체명현증강。결론 CPP가통과조체세포주기화유도조망발휘대인폐암QG56세포적억제작용。
Objective To investigate the inhibitory effects of periplocin from cortex periplocae (CPP) on human lung cancer cell line QG56 and to discuss its mechanism. Methods QG56 cells were cultured in vitro. The final concentrations of CPP in control group were 1.25, 2.50, 5.00, 10.00 and 20.00μg/L. QG56 cells were treated with ascending concentration of CPP for 24 h, 48 h and 72 h. The cell proliferation was measured using MTT method. The morphological changes of QG56 cells were observed under inverted microscope. Flow cytometry (FCM) was used to detect the effects of CPP on cell cycle and cell apoptosis. The expression of apoptosis associated gene bax mRNA in QG56 cells was detected by RT-PCR. The expres-sion of bax protein before and after treatment of CPP was examined by SP immunocytochemistry. Results The inhibitory ef-fect of CPP on the proliferation of QG56 cells was increased with the increasing concentrations of CPP and the prolonged du-ration of treatment. The morphological changes were displayed in QG56 exposed to CPP. The results of FCM showed that CPP caused cell cycle arrest at G0/G1 phase. The apoptotic rate of QG56 cells was significantly increased after CPP treatment for 48 h (P<0.05). The expression of bax mRNA was increased in QG56 exposed to CPP. The result of immunocytochemis-try indicated that CPP up-regulated the expression of bax protein. Conclusion CPP showed significant inhibitory effect on human lung cancer cell lines QG56 through inducing cell cycle arrest and apoptosis.